Perforation Peritonitis

Lt. Dhirendra

Case

• 60 yrs Female(1530hrs)

• c/o

– Pain abdomen

– Abdominal distension x2 days

• H/o

– Nausea and vomiting

– Not passing stool and flatus

– Loss of appetite

On Examination

• Afebrile

• P-104/min

• RR-20/min

• BP-114/72mmHg

• spO2-98%

• Pallor ++

• Tongue dry

• Pt.wt-44 kg

• Per Abdomen– Distension +

– Gen. guarding and tenderness +

– Tympanic note on percussion

– Liver dullness obliterated

– Bowel sounds absent

– Organs not palpable

– PR: rectum empty

• CVS

• Chest NAD

• CNS

On Investigations (2130hrs)• USG abdomen (civil)

– Free intraperitonial fluid with internal echoes

– ?Hollow viscous perforation

• CXR

– Free gas under diaphragm

• Haematology and Biochemistry

– Hb-13.6gm%

– TLC-16,300/cmm

– DLC – P85 L12 M1 E2

– Blood sugar(R)-84mg/dl

– B.Urea-64 mg/dl

– S.creatinine-2.0 mg/dl

– PT-15.5/16.5

– INR-1.11

Management

• Kept NPO

• Ryle’s tube

• Catheterization with Foley’s catheter

• Resuscitated with IV fluids

• IV antibiotics

• Pantoprazole

• Prepared for Exploratory Laparotomy

Exploratory Laparotomy (2330 hrs)

• Intra OP findings– Bilious peritoneal collection-1800ml

– 5mm perforation ant. aspect of 1st part of Duodenum

• Surgery– Peritoneal wash

– Grahm’s patch closure using 2/0 silk

– Drain placed

– Haemostasis ensured

Post OP management

• NPO

• IV fluids

• IV antibiotics

• Pantoprazole

• Epidural top up(morphine)

Patient gradually improved, orally started on 4th PO day, discharged on 12th PO day in satisfactory condition.

Discussion

Acute Abdomen

• Abdominal condition– abrupt onset

– severe abdominal pain

• Causes – Inflammation

– Obstruction

– Perforation

– Infarction

– Rupture of intra-abdominal organs

Peptic Ulcer Disease

• Focal defects

– gastric or duodenal mucosa

– extend into the submucosa or deeper

• Caused by an imbalance between mucosal defences and acid/peptic injury

Causative Agents

• Helicobacter Pylori infection

• Drugs (all NSAIDs,cocaine,etc)

• Smoking

• Alcohol

• Dietary habits

• Psychological stress

Pathogenesis

• Helicobacter pylori is implicated in 70–92% of all PUD

• The second most common cause-ingestion of NSAIDs.

• The least common cause is pathologic hypersecretory states, such as Zollinger-Ellison syndrome

Helicobacter Pylori• H.pylori possesses the enzyme urease:

– converts urea into ammonia and bicarbonate• The Bicarbonate buffers the acid secreted by the stomach.

• The ammonia is damaging to the SECs

• Inhibitory effect on antral D cells that secrete somatostatin– No inhibition of antral G-cell gastrin production

• Local alkalinisation of the antrum(antralacidification is the most potent antagonist to antral gastrin secretion)

• The end result is hypergastrinemia and acid hyper secretion

NSAID-Induced Disease

COMPLICATIONS OF PEPTIC ULCER DISEASE

• Bleeding

• Perforation

• Gastric Outlet Obstruction

• Intractable disease(Carcinoma)

Complications

• Upper GI bleeding-most common complication.

• Sudden large bleeding-life threatening.

• Occurs when the ulcer erodes blood vessels(gastroduodenal artery).

Perforation

• Most often chronic ulcer

• 50%: sealed off• Location: most often

anterior juxtapyloric• Mean diameter: 5mm

(>1cm=giant ulcer: rare)

• 10%: perforated gastric ulcer

Complications of Perforation

• Spillage of stomach or intestinal content into the abdominal cavity.

• Acute peritonitis– initially chemical

– later bacterial peritonitis(The first sign is sudden intense abdominal pain)

• Posterior wall perforation– Pancreatitis(pain radiates to the back)

– Perforation in the CBD- aerobilia, cholangitis

Signs and Symptoms

• Perforated Peptic ulcer

– Sudden-onset, severe, generalised abdominal pain

– Tachycardia

– Board-like rigidity

– Distension

– Obstipation

– Fever(not initially)

– Hypotension(later stage)

Diagnosis

• Perforated Peptic ulcer

– Erect plain chest radiograph

• free air can be seen in about 80% of cases

• CT imaging more accurate

– Amylase levels

• Rule out acute pancreatitis

Following resuscitation, the treatmentis principally surgical

• Laparotomy

• Laparoscopy

Component

– Thorough peritoneal toilet(remove fluid and food debris)

– Closing the ulcer (omental patch can be placed)

– Vagotomy (recently highly selective vagotomy)

– Systemic antibiotics

– Gastric anti-secretory agents

MinimallyInvasive Techniques

• Thorough peritoneal toilet

• Perforation closure by intracorporeal suturing

• Nasogastric suction

• Gastric anti-secretory agents

• Systemic antibiotics

• Patients who have suffered one perforation may suffer another one

– Eradication therapy for Helicobacter

– Lifelong treatment with proton pump inhibitors

Surgical management of peptic ulcer diseases• Vagotomy

– Truncal vagotomy and drainage

– highly selective vagotomy

– Truncal vagotomy and antrectomy

• Antrectomy

– Gastroduodenostomy(Billroth I)

– Gastrojejunostomy

(Billroth II)

In a nutshell

• Most peptic ulcers are caused by H. pylori or NSAIDs

• Common complications-perforation, bleeding and stenosis

• Diagnosis(perforation)-Erect plain chest radiograph(free air under diaphragm)

• The treatment of the perforated peptic ulcer is primarily surgical following resuscitation

• Gastric anti-secretory agents• Systemic antibiotics

Discussion